From the School of Social Work (Alcántara, Giorgio Cosenzo), Columbia University, New York, New York; Center for Behavioral Cardiovascular Health, Department of Medicine (Shimbo), Columbia University Medical Center, New York, New York; Institute for Policy Research and Department of Psychology (Leigh, Miller), Northwestern University, Evanston, Illinois.
Psychosom Med. 2019 Nov-Dec;81(9):778-781. doi: 10.1097/PSY.0000000000000745.
Adverse endothelial cell health, an early pathogenic process underlying atherosclerosis and cardiovascular disease, is evident in childhood and adolescence. Sleep duration, a modifiable cardiovascular health behavior, may be an important cardiovascular disease prevention target that may affect endothelial cell health. We examined the associations of longer sleep duration with endothelial cell injury among youth.
In a multiethnic sample of 235 children (63.0% female, mean age = 13.9 years), we conducted multivariable linear regressions to test the cross-sectional association of sleep duration and circulating levels of endothelial cell-derived microparticles (EMPs), phenotypic for endothelial cell activation and apoptosis (CD62E+ EMPs, CD31+/CD42b- EMPs, and CD31+/Annexin V+ EMPs). Sleep duration and EMPs were both treated as continuous variables. Models were adjusted for age, sex, race, pubertal status, household economic resources, and waist circumference.
Overall, 69.2% had short sleep duration (<8 hours of sleep per night). Longer sleep duration was significantly associated with lower levels of CD62E+ EMPs and CD31+/CD42b- EMPs. A 60-minute increase in sleep duration was associated with an 8.40 (95% confidence interval = -205.20 to -1.80, p = .046) decrease in CD62E+ EMPs and a 9.00 (95% confidence interval = -153.60 to -9.60, p = .027) decrease in CD31+/CD42b- EMPs. Sleep duration was not associated with CD31+/Annexin V+ EMPs.
Our results support the hypothesis that sleeping longer has beneficial effects on endothelial cell health during childhood. Primordial prevention efforts might incorporate sleep extension to offset cardiovascular risk in youth.
不良的内皮细胞健康是动脉粥样硬化和心血管疾病的早期发病机制，在儿童和青少年中就已经很明显。睡眠时长是一种可改变的心血管健康行为，它可能是一个重要的心血管疾病预防目标，可能会影响内皮细胞健康。我们研究了较长的睡眠时长与青少年内皮细胞损伤之间的关联。
在一个由 235 名儿童组成的多民族样本中（63.0%为女性，平均年龄为 13.9 岁），我们进行了多变量线性回归分析，以测试睡眠时长与内皮细胞衍生的微颗粒（EMPs）之间的横断面关联，这些微颗粒表型为内皮细胞激活和凋亡（CD62E+ EMPs、CD31+/CD42b- EMPs 和 CD31+/Annexin V+ EMPs）。睡眠时长和 EMPs 均被视为连续变量。模型调整了年龄、性别、种族、青春期状态、家庭经济资源和腰围。
总体而言，69.2%的儿童睡眠时间较短（每晚<8 小时）。较长的睡眠时长与较低水平的 CD62E+ EMPs 和 CD31+/CD42b- EMPs 显著相关。睡眠时长增加 60 分钟与 CD62E+ EMPs 降低 8.40（95%置信区间为-205.20 至-1.80，p =.046）和 CD31+/CD42b- EMPs 降低 9.00（95%置信区间为-153.60 至-9.60，p =.027）相关。睡眠时长与 CD31+/Annexin V+ EMPs 无关。
我们的结果支持这样的假设，即儿童时期睡眠时间较长对内皮细胞健康有益。原始预防措施可能会将睡眠延长纳入其中，以抵消青少年的心血管风险。
